What Is the Cause of ALS?

What Is the Cause of ALS?.jpeg

Lou Gehrig's disease, known as amyotrophic lateral sclerosis or ALS, strikes healthy, middle-aged people seemingly at random. Of the major neurodegenerative diseases, it has the least hope for treatment and survival. Although mental capabilities stay intact, ALS paralyzes people, often from the outside in, and most patients die within three years when they can no longer breathe or swallow. At any given time, an estimated 30,000 are fighting for their life with it in this country. We each have about a 1 in 400 chance of developing this dreaded disease.

ALS is more common than generally recognized, with an incidence rate now close to that of multiple sclerosis. What causes it? 50 years ago scientists found that the rate of ALS among the indigenous peoples on the island of Guam was 100 times that found in the rest of the world, potentially offering a clue into the cause of the disease. So instead of 1 in 400, in some villages in Guam, 1 in 3 adults died of the disease!

Cycad trees were suspected, since the powdered seeds were a dietary staple of the natives and there were reports of livestock showing neurological disease after eating from it. And indeed, a new neurotoxin was found in the seeds, called BMAA. Maybe that's what was causing such high levels of ALS? But the amount of BMAA in the seeds people ate was so small that it was calculated that people would have to eat a thousand kilograms a day to get a toxic dose--that's around a ton of seeds daily. So, the whole cycad theory was thrown out and the trail went cold.

But then famed neurologist Oliver Sachs and colleagues had an idea. Cycad seeds were not all the natives ate. They also ate fruit bats (also known as flying foxes) who ate Cycad tree seeds. So maybe this is a case of biomagnification up the food chain, as about a "tons" worth of BMAA does accumulate in the flesh of flying foxes.

The final nail in the coffin was the detection of high levels of BMMA in the brains of six out of six native victims of the disease on autopsy, but not in control brains of healthy people that died. So with the final puzzle piece apparently in place, the solution was found to this mysterious cluster on some exotic tropical isle of ALS/PDC, so-called because the form of ALS attacking people in Guam also had signs of Parkinson's disease and dementia, so they called it ALS parkinsonism dementia complex. So when the researchers were choosing a comparison group control brains, they also included two cases of Alzheimer's disease. But these brains had BMAA in their brains too. And not only that, but these were Alzheimer's victims in Canada, on the opposite side of the globe. So the researchers ran more autopsies and found no BMAA in the control brains, but BMAA detected in all the Canadian Alzheimer's victims tested.

Canadians don't eat fruit bats. What was going on? Well, the neurotoxin isn't made by the bat, it's made by the trees, although Canadians don't eat cycad trees either. It turns out that cycad trees don't make the neurotoxin either; it's actually a blue-green algae that grows in the roots of the cycad trees which makes the BMAA that gets in the seeds, which gets in the bats, that finally gets into the people. And it's not just this specific type of blue-green algae, but nearly all types of blue-green algae found all over the world produce BMAA. Up until only about a decade ago we thought this neurotoxin was confined to this one weird tropical tree, but now we know the neurotoxin is created by algae throughout the world; from Europe to the U.S., Australia, the Middle East, and elsewhere.

If these neurotoxin-producing blue-green algae are ubiquitous throughout the world, maybe BMAA is a cause of progressive neurodegenerative diseases including ALS worldwide. Researchers in Miami put it to the test and found BMAA in the brains of Floridians who died from sporadic Alzheimer's disease and ALS, but not in the brains of those that died of a different neurodegenerative disease called Huntington's, which we know is caused by a genetic mutation, not some neurotoxin. They found significant levels of BMAA in 49 out of 50 samples from 12 Alzheimer's patients and 13 ALS patients. The results (shown in the my video ALS: Fishing for Answers) for American Alzheimer's and ALS patients from the Atlantic southeast and from Canadian Alzheimer's patients from the Pacific Northwest suggested that exposure to BMAA was widespread. The same thing was then found in the brains of those dying from Parkinson's disease. You can apparently even pick up more BMAA in the hair of live ALS patients compared to controls.

So is BMAA present in Florida seafood? Yes, in freshwater fish and shellfish, like oysters and bass, and out in the ocean as well. Some of the fish, shrimp, and crabs had levels of BMAA comparable to those found in the fruit bats of Guam.

In the U.S., fish may be the fruit bats.

Maybe the ice bucket challenge should be to not serve seafood in them. See my video Diet and Amyotrophic Lateral Sclerosis (ALS) for more.

Diet may also play a role in other neurodegenerative disorders:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: GraphicStock. This image has been modified.

Original Link

What Is the Cause of ALS?

What Is the Cause of ALS?.jpeg

Lou Gehrig's disease, known as amyotrophic lateral sclerosis or ALS, strikes healthy, middle-aged people seemingly at random. Of the major neurodegenerative diseases, it has the least hope for treatment and survival. Although mental capabilities stay intact, ALS paralyzes people, often from the outside in, and most patients die within three years when they can no longer breathe or swallow. At any given time, an estimated 30,000 are fighting for their life with it in this country. We each have about a 1 in 400 chance of developing this dreaded disease.

ALS is more common than generally recognized, with an incidence rate now close to that of multiple sclerosis. What causes it? 50 years ago scientists found that the rate of ALS among the indigenous peoples on the island of Guam was 100 times that found in the rest of the world, potentially offering a clue into the cause of the disease. So instead of 1 in 400, in some villages in Guam, 1 in 3 adults died of the disease!

Cycad trees were suspected, since the powdered seeds were a dietary staple of the natives and there were reports of livestock showing neurological disease after eating from it. And indeed, a new neurotoxin was found in the seeds, called BMAA. Maybe that's what was causing such high levels of ALS? But the amount of BMAA in the seeds people ate was so small that it was calculated that people would have to eat a thousand kilograms a day to get a toxic dose--that's around a ton of seeds daily. So, the whole cycad theory was thrown out and the trail went cold.

But then famed neurologist Oliver Sachs and colleagues had an idea. Cycad seeds were not all the natives ate. They also ate fruit bats (also known as flying foxes) who ate Cycad tree seeds. So maybe this is a case of biomagnification up the food chain, as about a "tons" worth of BMAA does accumulate in the flesh of flying foxes.

The final nail in the coffin was the detection of high levels of BMMA in the brains of six out of six native victims of the disease on autopsy, but not in control brains of healthy people that died. So with the final puzzle piece apparently in place, the solution was found to this mysterious cluster on some exotic tropical isle of ALS/PDC, so-called because the form of ALS attacking people in Guam also had signs of Parkinson's disease and dementia, so they called it ALS parkinsonism dementia complex. So when the researchers were choosing a comparison group control brains, they also included two cases of Alzheimer's disease. But these brains had BMAA in their brains too. And not only that, but these were Alzheimer's victims in Canada, on the opposite side of the globe. So the researchers ran more autopsies and found no BMAA in the control brains, but BMAA detected in all the Canadian Alzheimer's victims tested.

Canadians don't eat fruit bats. What was going on? Well, the neurotoxin isn't made by the bat, it's made by the trees, although Canadians don't eat cycad trees either. It turns out that cycad trees don't make the neurotoxin either; it's actually a blue-green algae that grows in the roots of the cycad trees which makes the BMAA that gets in the seeds, which gets in the bats, that finally gets into the people. And it's not just this specific type of blue-green algae, but nearly all types of blue-green algae found all over the world produce BMAA. Up until only about a decade ago we thought this neurotoxin was confined to this one weird tropical tree, but now we know the neurotoxin is created by algae throughout the world; from Europe to the U.S., Australia, the Middle East, and elsewhere.

If these neurotoxin-producing blue-green algae are ubiquitous throughout the world, maybe BMAA is a cause of progressive neurodegenerative diseases including ALS worldwide. Researchers in Miami put it to the test and found BMAA in the brains of Floridians who died from sporadic Alzheimer's disease and ALS, but not in the brains of those that died of a different neurodegenerative disease called Huntington's, which we know is caused by a genetic mutation, not some neurotoxin. They found significant levels of BMAA in 49 out of 50 samples from 12 Alzheimer's patients and 13 ALS patients. The results (shown in the my video ALS: Fishing for Answers) for American Alzheimer's and ALS patients from the Atlantic southeast and from Canadian Alzheimer's patients from the Pacific Northwest suggested that exposure to BMAA was widespread. The same thing was then found in the brains of those dying from Parkinson's disease. You can apparently even pick up more BMAA in the hair of live ALS patients compared to controls.

So is BMAA present in Florida seafood? Yes, in freshwater fish and shellfish, like oysters and bass, and out in the ocean as well. Some of the fish, shrimp, and crabs had levels of BMAA comparable to those found in the fruit bats of Guam.

In the U.S., fish may be the fruit bats.

Maybe the ice bucket challenge should be to not serve seafood in them. See my video Diet and Amyotrophic Lateral Sclerosis (ALS) for more.

Diet may also play a role in other neurodegenerative disorders:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: GraphicStock. This image has been modified.

Original Link

Why Is Milk Consumption Associated with More Bone Fractures?

Why Is Milk Consumption Associated with More Bone Fractures?.jpg

Milk is touted to build strong bones, but a compilation of all the best studies found no association between milk consumption and hip fracture risk, so drinking milk as an adult might not help bones, but what about in adolescence? Harvard researchers decided to put it to the test.

Studies have shown that greater milk consumption during childhood and adolescence contributes to peak bone mass, and is therefore expected to help avoid osteoporosis and bone fractures in later life. But that's not what researchers have found (as you can see in my video Is Milk Good for Our Bones?). Milk consumption during teenage years was not associated with a lower risk of hip fracture, and if anything, milk consumption was associated with a borderline increase in fracture risk in men.

It appears that the extra boost in total body bone mineral density from getting extra calcium is lost within a few years; even if you keep the calcium supplementation up. This suggests a partial explanation for the long-standing enigma that hip fracture rates are highest in populations with the greatest milk consumption. This may be an explanation for why they're not lower, but why would they be higher?

This enigma irked a Swedish research team, puzzled because studies again and again had shown a tendency of a higher risk of fracture with a higher intake of milk. Well, there is a rare birth defect called galactosemia, where babies are born without the enzymes needed to detoxify the galactose found in milk, so they end up with elevated levels of galactose in their blood, which can causes bone loss even as kids. So maybe, the Swedish researchers figured, even in normal people that can detoxify the stuff, it might not be good for the bones to be drinking it every day.

And galactose doesn't just hurt the bones. Galactose is what scientists use to cause premature aging in lab animals--it can shorten their lifespan, cause oxidative stress, inflammation, and brain degeneration--just with the equivalent of like one to two glasses of milk's worth of galactose a day. We're not rats, though. But given the high amount of galactose in milk, recommendations to increase milk intake for prevention of fractures could be a conceivable contradiction. So, the researchers decided to put it to the test, looking at milk intake and mortality as well as fracture risk to test their theory.

A hundred thousand men and women were followed for up to 20 years. Researchers found that milk-drinking women had higher rates of death, more heart disease, and significantly more cancer for each glass of milk. Three glasses a day was associated with nearly twice the risk of premature death, and they had significantly more bone and hip fractures. More milk, more fractures.

Men in a separate study also had a higher rate of death with higher milk consumption, but at least they didn't have higher fracture rates. So, the researchers found a dose dependent higher rate of both mortality and fracture in women, and a higher rate of mortality in men with milk intake, but the opposite for other dairy products like soured milk and yogurt, which would go along with the galactose theory, since bacteria can ferment away some of the lactose. To prove it though, we need a randomized controlled trial to examine the effect of milk intake on mortality and fractures. As the accompanying editorial pointed out, we better find this out soon since milk consumption is on the rise around the world.

What can we do for our bones, then? Weight-bearing exercise such as jumping, weight-lifting, and walking with a weighted vest or backpack may help, along with getting enough calcium (Alkaline Diets, Animal Protein, & Calcium Loss) and vitamin D (Resolving the Vitamin D-Bate). Eating beans (Phytates for the Prevention of Osteoporosis) and avoiding phosphate additives (Phosphate Additives in Meat Purge and Cola) may also help.

Maybe the galactose angle can help explain the findings on prostate cancer (Prostate Cancer and Organic Milk vs. Almond Milk) and Parkinson's disease (Preventing Parkinson's Disease With Diet).

Galactose is a milk sugar. There's also concern about milk proteins (see my casomorphin series) and fats (The Saturated Fat Studies: Buttering Up the Public and Trans Fat in Meat and Dairy) as well as the hormones (Dairy Estrogen and Male Fertility, Estrogen in Meat, Dairy, and Eggs and Why Do Vegan Women Have 5x Fewer Twins?).

Milk might also play a role in diabetes (Does Casein in Milk Trigger Type 1 Diabetes, Does Bovine Insulin in Milk Trigger Type 1 Diabetes?) and breast cancer (Is Bovine Leukemia in Milk Infectious?, The Role of Bovine Leukemia Virus in Breast Cancer, and Industry Response to Bovine Leukemia Virus in Breast Cancer).

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

Why Is Milk Consumption Associated with More Bone Fractures?

Why Is Milk Consumption Associated with More Bone Fractures?.jpg

Milk is touted to build strong bones, but a compilation of all the best studies found no association between milk consumption and hip fracture risk, so drinking milk as an adult might not help bones, but what about in adolescence? Harvard researchers decided to put it to the test.

Studies have shown that greater milk consumption during childhood and adolescence contributes to peak bone mass, and is therefore expected to help avoid osteoporosis and bone fractures in later life. But that's not what researchers have found (as you can see in my video Is Milk Good for Our Bones?). Milk consumption during teenage years was not associated with a lower risk of hip fracture, and if anything, milk consumption was associated with a borderline increase in fracture risk in men.

It appears that the extra boost in total body bone mineral density from getting extra calcium is lost within a few years; even if you keep the calcium supplementation up. This suggests a partial explanation for the long-standing enigma that hip fracture rates are highest in populations with the greatest milk consumption. This may be an explanation for why they're not lower, but why would they be higher?

This enigma irked a Swedish research team, puzzled because studies again and again had shown a tendency of a higher risk of fracture with a higher intake of milk. Well, there is a rare birth defect called galactosemia, where babies are born without the enzymes needed to detoxify the galactose found in milk, so they end up with elevated levels of galactose in their blood, which can causes bone loss even as kids. So maybe, the Swedish researchers figured, even in normal people that can detoxify the stuff, it might not be good for the bones to be drinking it every day.

And galactose doesn't just hurt the bones. Galactose is what scientists use to cause premature aging in lab animals--it can shorten their lifespan, cause oxidative stress, inflammation, and brain degeneration--just with the equivalent of like one to two glasses of milk's worth of galactose a day. We're not rats, though. But given the high amount of galactose in milk, recommendations to increase milk intake for prevention of fractures could be a conceivable contradiction. So, the researchers decided to put it to the test, looking at milk intake and mortality as well as fracture risk to test their theory.

A hundred thousand men and women were followed for up to 20 years. Researchers found that milk-drinking women had higher rates of death, more heart disease, and significantly more cancer for each glass of milk. Three glasses a day was associated with nearly twice the risk of premature death, and they had significantly more bone and hip fractures. More milk, more fractures.

Men in a separate study also had a higher rate of death with higher milk consumption, but at least they didn't have higher fracture rates. So, the researchers found a dose dependent higher rate of both mortality and fracture in women, and a higher rate of mortality in men with milk intake, but the opposite for other dairy products like soured milk and yogurt, which would go along with the galactose theory, since bacteria can ferment away some of the lactose. To prove it though, we need a randomized controlled trial to examine the effect of milk intake on mortality and fractures. As the accompanying editorial pointed out, we better find this out soon since milk consumption is on the rise around the world.

What can we do for our bones, then? Weight-bearing exercise such as jumping, weight-lifting, and walking with a weighted vest or backpack may help, along with getting enough calcium (Alkaline Diets, Animal Protein, & Calcium Loss) and vitamin D (Resolving the Vitamin D-Bate). Eating beans (Phytates for the Prevention of Osteoporosis) and avoiding phosphate additives (Phosphate Additives in Meat Purge and Cola) may also help.

Maybe the galactose angle can help explain the findings on prostate cancer (Prostate Cancer and Organic Milk vs. Almond Milk) and Parkinson's disease (Preventing Parkinson's Disease With Diet).

Galactose is a milk sugar. There's also concern about milk proteins (see my casomorphin series) and fats (The Saturated Fat Studies: Buttering Up the Public and Trans Fat in Meat and Dairy) as well as the hormones (Dairy Estrogen and Male Fertility, Estrogen in Meat, Dairy, and Eggs and Why Do Vegan Women Have 5x Fewer Twins?).

Milk might also play a role in diabetes (Does Casein in Milk Trigger Type 1 Diabetes, Does Bovine Insulin in Milk Trigger Type 1 Diabetes?) and breast cancer (Is Bovine Leukemia in Milk Infectious?, The Role of Bovine Leukemia Virus in Breast Cancer, and Industry Response to Bovine Leukemia Virus in Breast Cancer).

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

The Mediterranean Diet or a Whole Food Plant-Based Diet?

The Mediterranean Diet or a Whole Food Plant-Based Diet.jpg

Recent studies have shown that higher Mediterranean diet adherence scores are associated with a significant reduction of the risk of death, heart disease, cancer, and brain disease. The problem with population studies like these is that people who eat healthier may also live healthier, and so how do we know it's their diet? I examine this in The Mediterranean Diet or a Whole Food Plant-Based Diet?.

As the American Heart Association position states, "Before advising people to follow a Mediterranean diet, we need more studies to find out whether the diet itself or other lifestyle factors account for the lower deaths from heart disease." How do you do that? There are ways you can control for obvious things like smoking and exercise--which many of the studies did--but ideally you'd do an interventional trial, the gold standard of nutritional science. You change people's diets while trying to keep everything else the same and see what happens.

We got that kind of trial 20 years ago with the famous Lyon Diet Heart Study where about 600 folks who had just had their first heart attack were randomized into two groups. The control group received no dietary advice, apart whatever their doctors were telling them, while the experimental group was told to eat more of a Mediterranean-type diet, supplemented with a canola-oil based spread to give them the plant-based omega-3's they'd normally be getting from weeds and walnuts if they actually lived on a Greek isle in the 1950's.

The Mediterranean diet group did end up taking some of the dietary advice to heart. They ate more bread, more fruit, less deli meat, less meat in general, and less butter and cream; other than that, no significant changes in diet were reported in terms of wine, olive oil, or fish consumption. So, they ate less saturated fat and cholesterol, more plant-based omega 3's, but didn't have huge dietary changes. Even so, at the end of about four years, 44 individuals from the control group had a second heart attack, either fatal or nonfatal, but only 14 suffered another attack in the group that changed their diet. So they went from having a 4% chance of having a heart attack every year down to 1%.

A cynic might say that while there was less death and disease, the Mediterranean diet continued to feed their heart disease, so much so that 14 of them suffered new heart attacks while on the diet. Yes, their disease progressed a lot less than the regular diet group (about four times less), but what if there was a diet that could stop or reverse heart disease?

Dr. Caldwell Esselstyn and colleagues at the Cleveland Clinic recently published a case series of 198 consecutive patients with cardiovascular disease counseled to switch to a diet composed entirely of whole plant foods. Of the 198, 177 stuck to the diet, whereas the other 21 fell off the wagon, setting up kind of a natural experiment. What happened to the 21? This was such a sick group of patients that more than half suffered from either a fatal heart attack or needed angioplasty or a heart transplant. In that same time period of about four years, of the 177 that stuck to the plant-based diet, only one had a major event as a result of worsening disease. As Dean Ornish noted in his response to the latest trial, "a Mediterranean diet is better than what most people are consuming"...but even better may be a diet based on whole plant foods.

Dr. Esselstyn's was not a randomized trial, so it can't be directly compared to the Lyon study, and it included very determined patients. Not everyone is willing to dramatically change their diets, even if it may literally be a matter of life or death. In which case, rather than doing nothing, eating a more Mediterranean-type diet may cut risk for heart attack survivors by about two-thirds. Cutting 99% of risk would be better if Esselstyn's results were replicated in a controlled trial, but even a 70% drop in risk could save tens of thousands of lives every year.

For more on the Mediterranean diet, check out:

For more on Dr. Esselstyn's amazing work:

If the short-chain plant-based omega-3s in flax seeds and walnuts appear so beneficial, what about the long-chain omega-3's found in fish and fish oil? There are pros and cons. See, for example, Mercury vs. Omega-3s for Brain Development, Is Fish Oil Just Snake Oil?, and Omega-3's and the Eskimo Fish Tale.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: wildpixel / Thinkstock. This image has been modified.

Original Link

The Mediterranean Diet or a Whole Food Plant-Based Diet?

The Mediterranean Diet or a Whole Food Plant-Based Diet.jpg

Recent studies have shown that higher Mediterranean diet adherence scores are associated with a significant reduction of the risk of death, heart disease, cancer, and brain disease. The problem with population studies like these is that people who eat healthier may also live healthier, and so how do we know it's their diet? I examine this in The Mediterranean Diet or a Whole Food Plant-Based Diet?.

As the American Heart Association position states, "Before advising people to follow a Mediterranean diet, we need more studies to find out whether the diet itself or other lifestyle factors account for the lower deaths from heart disease." How do you do that? There are ways you can control for obvious things like smoking and exercise--which many of the studies did--but ideally you'd do an interventional trial, the gold standard of nutritional science. You change people's diets while trying to keep everything else the same and see what happens.

We got that kind of trial 20 years ago with the famous Lyon Diet Heart Study where about 600 folks who had just had their first heart attack were randomized into two groups. The control group received no dietary advice, apart whatever their doctors were telling them, while the experimental group was told to eat more of a Mediterranean-type diet, supplemented with a canola-oil based spread to give them the plant-based omega-3's they'd normally be getting from weeds and walnuts if they actually lived on a Greek isle in the 1950's.

The Mediterranean diet group did end up taking some of the dietary advice to heart. They ate more bread, more fruit, less deli meat, less meat in general, and less butter and cream; other than that, no significant changes in diet were reported in terms of wine, olive oil, or fish consumption. So, they ate less saturated fat and cholesterol, more plant-based omega 3's, but didn't have huge dietary changes. Even so, at the end of about four years, 44 individuals from the control group had a second heart attack, either fatal or nonfatal, but only 14 suffered another attack in the group that changed their diet. So they went from having a 4% chance of having a heart attack every year down to 1%.

A cynic might say that while there was less death and disease, the Mediterranean diet continued to feed their heart disease, so much so that 14 of them suffered new heart attacks while on the diet. Yes, their disease progressed a lot less than the regular diet group (about four times less), but what if there was a diet that could stop or reverse heart disease?

Dr. Caldwell Esselstyn and colleagues at the Cleveland Clinic recently published a case series of 198 consecutive patients with cardiovascular disease counseled to switch to a diet composed entirely of whole plant foods. Of the 198, 177 stuck to the diet, whereas the other 21 fell off the wagon, setting up kind of a natural experiment. What happened to the 21? This was such a sick group of patients that more than half suffered from either a fatal heart attack or needed angioplasty or a heart transplant. In that same time period of about four years, of the 177 that stuck to the plant-based diet, only one had a major event as a result of worsening disease. As Dean Ornish noted in his response to the latest trial, "a Mediterranean diet is better than what most people are consuming"...but even better may be a diet based on whole plant foods.

Dr. Esselstyn's was not a randomized trial, so it can't be directly compared to the Lyon study, and it included very determined patients. Not everyone is willing to dramatically change their diets, even if it may literally be a matter of life or death. In which case, rather than doing nothing, eating a more Mediterranean-type diet may cut risk for heart attack survivors by about two-thirds. Cutting 99% of risk would be better if Esselstyn's results were replicated in a controlled trial, but even a 70% drop in risk could save tens of thousands of lives every year.

For more on the Mediterranean diet, check out:

For more on Dr. Esselstyn's amazing work:

If the short-chain plant-based omega-3s in flax seeds and walnuts appear so beneficial, what about the long-chain omega-3's found in fish and fish oil? There are pros and cons. See, for example, Mercury vs. Omega-3s for Brain Development, Is Fish Oil Just Snake Oil?, and Omega-3's and the Eskimo Fish Tale.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: wildpixel / Thinkstock. This image has been modified.

Original Link

Reducing Glycotoxin Intake to Help Reduce Brain Loss

Reducing Glycotoxin Intake to Prevent Alzheimer's.jpg

Each of us has about six billion miles of DNA. How does our body keep it from getting all tangled up? There are special proteins called histones, which act like spools with DNA as the thread. Enzymes called sirtuins wrap the DNA around the histones and by doing so, silence whatever genes were in that stretch of DNA, hence their name SIRtuins, which stands for silencing information regulator.

Although they were discovered only about a decade ago, the study of sirtuins "has become one of the most promising areas of biomedicine," since they appear to be involved in promoting healthy aging and longevity. Suppression of this key host defense is considered a central feature of Alzheimer's disease, as shown in Reducing Glycotoxin Intake to Prevent Alzheimer's.

Autopsies of Alzheimer's victims reveal that loss of sirtuin activity is closely associated with the accumulation of the plaques and tangles in the brain that are characteristic of Alzheimer's disease. Sirtuin appears to activate pathways that steer the brain away from the formation of plaque and tangle proteins. "Because a decrease in sirtuin activity can clearly have deleterious effects" on nerve health, researchers are trying to come up with drugs to increase sirtuin activity, but why not just prevent its suppression in the first place?

Glycotoxins in our food suppress sirtuin activity, also known as advanced glycation end products, or AGE's. Our modern diet includes excessive AGE's, which can be neurotoxic. High levels in the blood may predict cognitive decline over time. If you measure the urine levels of glycotoxins flowing through the bodies of older adults, those with the highest levels went on to suffer the greatest cognitive decline over the subsequent nine years.

As we age, our brain literally shrinks. In our 60's and 70's, we lose an average of five cubic centimeters of total brain tissue volume every year, but some people lose more than others. Brain atrophy may be reduced in very healthy individuals, and a few people don't lose any brain at all. Normally we lose about 2% of brain volume every year, but that's just the average. Although the average brain loss for folks in their 70's and 80's was 2.1%, some lost more, some lost less, and some men and women lost none at all over a period of four years.

Researchers in Australia provided the first evidence linking AGEs with this kind of cerebral brain loss. So, limiting one's consumption of these compounds may end up having significant public health benefits. Because sirtuin deficiency is both preventable and reversible by dietary AGE reduction, a therapeutic strategy that includes eating less AGE's may offer a new strategy to combat the epidemic of Alzheimer's.

Some glycotoxins are produced internally, particularly in diabetics, but anyone can get them from smoking and eating, particularly foods high in fat and protein cooked at high temperatures. In my video, Avoiding a Sugary Grave, I listed the 15 foods most contaminated with glycotoxins; mostly chicken, but also pork, beef, and fish, which may help explain why those that eat the most meat may have triple the risk of getting dementia compared to long-time vegetarians. Note there are some relatively high fat and protein plant foods such as nuts and soy products, so I no longer recommend toasting nuts and would steer clear from roasted tofu.

I've covered advanced glycation end-products in Glycotoxins, Bacon, Eggs, and Gestational Diabetes During Pregnancy, and Why is Meat a Risk Factor for Diabetes?.

More on slowing brain aging in How to Slow Brain Aging By Two Years.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: lightwise © 123RF.com. This image has been modified.

Original Link

Reducing Glycotoxin Intake to Help Reduce Brain Loss

Reducing Glycotoxin Intake to Prevent Alzheimer's.jpg

Each of us has about six billion miles of DNA. How does our body keep it from getting all tangled up? There are special proteins called histones, which act like spools with DNA as the thread. Enzymes called sirtuins wrap the DNA around the histones and by doing so, silence whatever genes were in that stretch of DNA, hence their name SIRtuins, which stands for silencing information regulator.

Although they were discovered only about a decade ago, the study of sirtuins "has become one of the most promising areas of biomedicine," since they appear to be involved in promoting healthy aging and longevity. Suppression of this key host defense is considered a central feature of Alzheimer's disease, as shown in Reducing Glycotoxin Intake to Prevent Alzheimer's.

Autopsies of Alzheimer's victims reveal that loss of sirtuin activity is closely associated with the accumulation of the plaques and tangles in the brain that are characteristic of Alzheimer's disease. Sirtuin appears to activate pathways that steer the brain away from the formation of plaque and tangle proteins. "Because a decrease in sirtuin activity can clearly have deleterious effects" on nerve health, researchers are trying to come up with drugs to increase sirtuin activity, but why not just prevent its suppression in the first place?

Glycotoxins in our food suppress sirtuin activity, also known as advanced glycation end products, or AGE's. Our modern diet includes excessive AGE's, which can be neurotoxic. High levels in the blood may predict cognitive decline over time. If you measure the urine levels of glycotoxins flowing through the bodies of older adults, those with the highest levels went on to suffer the greatest cognitive decline over the subsequent nine years.

As we age, our brain literally shrinks. In our 60's and 70's, we lose an average of five cubic centimeters of total brain tissue volume every year, but some people lose more than others. Brain atrophy may be reduced in very healthy individuals, and a few people don't lose any brain at all. Normally we lose about 2% of brain volume every year, but that's just the average. Although the average brain loss for folks in their 70's and 80's was 2.1%, some lost more, some lost less, and some men and women lost none at all over a period of four years.

Researchers in Australia provided the first evidence linking AGEs with this kind of cerebral brain loss. So, limiting one's consumption of these compounds may end up having significant public health benefits. Because sirtuin deficiency is both preventable and reversible by dietary AGE reduction, a therapeutic strategy that includes eating less AGE's may offer a new strategy to combat the epidemic of Alzheimer's.

Some glycotoxins are produced internally, particularly in diabetics, but anyone can get them from smoking and eating, particularly foods high in fat and protein cooked at high temperatures. In my video, Avoiding a Sugary Grave, I listed the 15 foods most contaminated with glycotoxins; mostly chicken, but also pork, beef, and fish, which may help explain why those that eat the most meat may have triple the risk of getting dementia compared to long-time vegetarians. Note there are some relatively high fat and protein plant foods such as nuts and soy products, so I no longer recommend toasting nuts and would steer clear from roasted tofu.

I've covered advanced glycation end-products in Glycotoxins, Bacon, Eggs, and Gestational Diabetes During Pregnancy, and Why is Meat a Risk Factor for Diabetes?.

More on slowing brain aging in How to Slow Brain Aging By Two Years.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: lightwise © 123RF.com. This image has been modified.

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How May Eating Plants Help Prevent Alzheimer’s Disease?

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Intake of saturated fats and added sugars, two of the primary components of a modern Western diet, is linked with the development of Alzheimer's disease. There has been a global shift in dietary composition, from traditional diets high in starches and fiber, to what has been termed the Western diet, high in fat and sugar, low in whole, plant foods. What's so great about fruits and vegetables?

Plant-derived foods contain thousands of compounds with antioxidant properties, some of which can traverse the blood-brain barrier and may have neuroprotective effects by assisting with antioxidant defense. There's this concept of "brain rust," that neurodegenerative diseases arise from excess oxidative stress. But Nature has gifted humankind with a plethora of plants--fruits, vegetables, and nuts, and the diverse array of bioactive nutrients present in these natural products may play a pivotal role in prevention and one day, perhaps, even the cure of various neurodegenerative diseases, such as Alzheimer's disease.

Accumulated evidence suggests that naturally occurring plant compounds may potentially hinder neurodegeneration, and even improve memory and cognitive function, as I've shared in my videos Preventing Alzheimer's Disease with Plants and How to Slow Brain Aging By Two Years) and treating Alzheimer's with spices such as saffron or turmeric (See Saffron for the Treatment of Alzheimer's and Treating Alzheimer's with Turmeric).

Vegetables may be particularly protective, in part because of certain compounds we eat that concentrate in the brain, found in dark green leafy vegetables, the consumption of which are associated with lower rates of age-related cognitive decline.

Yet when you look at systemic reviews on what we can do to prevent cognitive decline, you'll see conclusions like this: "The current literature does not provide adequate evidence to make recommendations for interventions." The same is said for Alzheimer's, "Currently, insufficient evidence exists to draw firm conclusions on the association of any modifiable factors with risk of Alzheimer's disease." Doctors cite the lack of randomized controlled trials (RCTs) as the basis for their conclusions. RCTs are the gold standard used to test new medicines. This is where researchers randomize people into two groups, half get the drug and half don't, to control for confounding factors. The highest level of evidence is necessary because drugs may kill a hundred thousand Americans every year - not medication errors or illicit drugs, just regular, FDA-approved prescription drugs, making medication alone the sixth leading cause of death in the United States. So, you better make absolutely sure the benefits of new drugs outweigh the often life-threatening risks.

But we're talking about diet and exercise--the side effects are all good, so we don't need the same level of rigorous evidence to prescribe them.

A "modest proposal" was published recently in the Journal of Alzheimer's Disease, an editorial calling for a longitudinal study of dementia prevention. They agreed that definitive evidence for the effectiveness of dementia prevention methods was lacking, so we need large-scaled randomized trials. They suggested we start with 10,000 healthy volunteers in their 20's and split them into five groups. There's evidence, for example, that traumatic brain injury is a risk factor for Alzheimer's, because people with head injuries appear more likely to get the disease, but it's never been put to the test. So, they say, let's take two thousand people and beat half of them in the head with baseball bats, and the other half we'll use Styrofoam bats as a control. Afterall, until we have randomized controls, how can't physicians recommend patients not get hit in the head? They go further saying we should probably chain a thousand people to a treadmill for 40 years, and a thousand people to a couch before recommending exercise. A thousand will be forced to do crossword puzzles; another thousand forced to watch Jerry Springer reruns, lots of meat and dairy or not prescribed for another group for the next 40 years, and we can hook a thousand folks on four packs a day just to be sure.

We help our patients to quit smoking despite the fact that there's not a single randomized controlled trial where they held people down and piped smoke into their lungs for a few decades. It is time to realize that the ultimate study in regard to lifestyle and cognitive health cannot be done. Yet the absence of definitive evidence should not restrict physicians from making reasonable recommendations based on the evidence that is available.

I've discussed how drug-centric approaches to evidence-based medicine may neglect some of the most convincing data: Evidence-Based Medicine or Evidence-Biased?

To see how and why I built NutritionFacts.org on evidence-based principles, see my recent introductory videos:

A sampling of some of my Alzheimer's videos:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations--2013: Uprooting the Leading Causes of Death, More Than an Apple a Day, 2014: From Table to Able: Combating Disabling Diseases with Food, 2015: Food as Medicine: Preventing and Treating the Most Dreaded Diseases with Diet, and my latest, 2016: How Not To Die: The Role of Diet in Preventing, Arresting, and Reversing Our Top 15 Killers.

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How to Mitigate and Prevent Crohn’s Disease with Diet

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Crohn's disease is an autoimmune disorder that affects more than a million Americans. It is an inflammatory bowel disease in which the body attacks the intestines. There is currently no known cure for Crohn's disease; current research focuses on controlling symptoms. There is no definitive medical or surgical therapy. The best we have is a plant-based diet, which has afforded the best relapse prevention to date.

Researchers got the idea to try a plant-based diet because diets rich in animal protein and animal fat have been found to cause a decrease in beneficial bacteria in the intestine. So, researchers designed a semi-vegetarian diet to counter that, and 100 percent of subjects stayed in remission the first year and 92 percent the second year. These results are far better than those obtained by current drugs, including new "biological agents" that can cost $40,000 a year, and can cause progressive multifocal leukoencephalopathy, a disabling and deadly brain disease. And a healthy diet appears to work better.

But what about preventing Crohn's disease in the first place? A systematic review of the scientific literature on dietary intake and the risk of developing inflammatory bowel disease found that a high intake of fats and meat was associated with an increased risk of Crohn's disease as well as ulcerative colitis, whereas high fiber and fruit intakes were associated with decreased risk of Crohn's.

These results were supported more recently by the Harvard Nurse's Health Study. Data revealed that long-term intake of dietary fiber, particularly from fruit, was associated with lower risk of Crohn's disease. Women who fell into in the highest long-term fiber consumption group had a 40 percent reduced risk, leading the accompanying editorial to conclude, "advocating for a high-fiber diet may ultimately reduce the incidence of Crohn's disease."

The irony is that the highest fiber group wasn't even eating the official recommended daily minimum of fiber intake. Apparently, even just being less fiber deficient has a wide range of benefits, including a significant reduction in the risk of developing Crohn's disease, but why? The authors suggest it's because "fiber plays a vital role in the maintenance of our intestinal barrier function."

Our skin keeps the outside world outside, and so does the lining of our gut, but in Crohn's disease, this barrier function is impaired. You can see this under an electron microscope as shown in my video Preventing Crohn's Disease With Diet. The tight junctions between the intestinal cells have all sorts of little holes and breaks. The thought is that the increase in prevalence of inflammatory bowel diseases may be that dietary changes lead to the breakdown of our intestinal barrier, potentially allowing the penetration of bacteria into our gut wall, which our body then attacks, triggering the inflammation.

We know fiber acts as a prebiotic in our colon (large intestine), feeding our good bacteria, but what does fiber do in our small intestine where Crohn's often starts? We didn't know, until a landmark study was published. Researchers wanted to find out what could stop Crohn's associated invasive bacteria from tunneling into the gut wall. They found the invasion is inhibited by the presence of certain soluble plant fibers, such as from plantains and broccoli at the kinds of concentrations one might expect after eating them. They wondered if that may explain why plantain-loving populations have lower levels of inflammatory bowel disease. But, the researchers also found that there was something in processed foods that facilitated the invasion of the bacteria. Polysorbate 80 was one of them, found predominantly in ice cream, but also found in Crisco, Cool Whip, condiments, cottage cheese--you just have to read the labels.

What about maltodextrin, which is found in artificial sweeteners like Splenda, snack foods, salad dressings, and fiber supplements? Maltodextrin markedly enhanced the ability of the bacteria to glob onto our intestinal cells, though other additives. Carboxy-methyl cellulose and xanthan gum appeared to have no adverse effects.

This may all help solve the mystery of the increasing prevalence of Crohn's disease in developed nations, where we're eating less fiber-containing whole plant foods and more processed foods. What we need now are interventional studies to see if boosting fiber intake and avoiding these food additives can be effective in preventing and treating Crohn's disease. But until then, what do we tell people? The available evidence points to a diet low in animal fat, with lots of soluble fiber containing plant foods, and avoiding processed fatty foods that contain these emulsifiers. We also want to make sure we're not ingesting traces of dishwashing detergent, which could have the same effect, so make sure to rinse your dishes well. Researchers found that some people wash dishes and then just leave them to dry without rinsing, which is probably not a good idea. We don't currently have studies that show that avoiding polysorbate 80 and rinsing dishes well actually helps. Nevertheless, advice based on 'best available evidence' is better than no advice at all.

Here's a video about using a more plant-based diet to reduce the risk of relapses: Dietary Treatment of Crohn's Disease.

I get a lot of questions about additives like polysorbate 80. I'm glad I was finally able to do a blog about it. Here are some videos on some others:

If you, like me, used to think all fiber was good for was helping with bowel regularity you'll be amazed! See for example, Dr. Burkitt's F-Word Diet.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations--2013: Uprooting the Leading Causes of Death, More Than an Apple a Day, 2014: From Table to Able: Combating Disabling Diseases with Food, 2015: Food as Medicine: Preventing and Treating the Most Dreaded Diseases with Diet, and my latest, 2016: How Not To Die: The Role of Diet in Preventing, Arresting, and Reversing Our Top 15 Killers.

Image Credit: Graphic Stock

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